The ability of Candida albicans to cause disease is associated with its capacity to undergo morphological transition between yeast and filamentous forms, but the role of morphology in colonisation and dissemination from the gastrointestinal (GI) tract remains poorly defined. To explore this, we made use of wild type and morphological mutants of C. albicans in an established model of GI tract colonization, induced following antibiotic-treatment of mice. Our data reveal that GI tract colonization favours the yeast form of C. albicans, that there is constitutive low level systemic dissemination in colonized mice that occurs irrespective of fungal morphology, and that colonization is not controlled by Th17 immunity in otherwise immunocompetent animals. These data provide new insights into the mechanisms of pathogenesis and commensalism of C. albicans, and have implications for our understanding of human disease.
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This work was supported by the Wellcome Trust (086558, 080088, 102705), a
Wellcome Trust Strategic Award (097377) and a studentship from the University of
Aberdeen. D.K. was supported by grant 5R01AI083344 from the National Institute of Allergy and Infectious Diseases and by a Voelcker Young Investigator Award from
the Max and Minnie Tomerlin Voelcker Fund.